目的 研究莱菔硫烷对人肝癌HepG2细胞Fas、FasL、Bid蛋白表达的影响，探讨其诱导HepG2细胞凋亡过程中Fas/FasL途径的作用。方法 Caspase-8试剂盒检测莱菔硫烷对HepG2细胞Caspase-8活性的影响；流式细胞仪检测莱菔硫烷对HepG2细胞中Fas、FasL、Bid蛋白表达的影响。结果 莱菔硫烷10、20、40 μmol/L作用于HepG2细胞48 h，可显著升高HepG2细胞Caspase-8活性（P＜0.01）；可使HepG2细胞 Fas、FasL蛋白的表达显著升高（P＜0.01）；莱菔硫烷20、40 μmol/L时，可显著提高Bid蛋白的表达（P＜0.01），上述作用均呈剂量相关性。结论 激活Fas/FasL途径可能是莱菔硫烷诱导人肝癌HepG2细胞凋亡的重要机制之一。

Objective To study the effect of sulforaphane on Fas, FasL, and Bid protein expression in HepG2 cells, and to explore the effect of Fas/FasL pathway on sulforaphane-induced apoptosis in HepG2 cells. Methods The effect of sulforaphane on Caspase-8 activity in HepG2 cells was detected by Caspase-8 Activity Assay Kit. Flow cytometer was used to analysis of Fas, FasL, and Bid protein expression in HepG2 cells. Results After treated by sulforaphane for 48 h, the Caspase-8 activity was effectively increased (P<0.01). At the doses of 10, 20 and 40 μmol/L, the effect of sulforaphane could significantly increase the Fas and FasL protein expression in HepG2 cells in a dose dependent manner, while at the doses of 20 and 40 μmol/L, sulforaphane could increase the Bid protein expression. Conclusion Activating the Fas/FasL pathway may be one of the role mechanism of sulforaphane inducing the apoptosis of HepG2 cells.

国家自然科学基金资助项目（30300284）；黑龙江省自然科学基金重大项目（ZJY03-04；D200802）